EXO1 (Exonuclease 1)

Functional assays in both T47D and MCF7 cells demonstrated that co-expression of N4BP2L2 restored HR activity and reduced olaparib sensitivity in EXO1-overexpressing cells. These findings suggest EXO1 overexpression serves as a marker of functional HR deficiency and a potential predictor of PARP inhibitor response, highlighting the EXO1-N4BP2L2 axis as a promising biomarker and therapeutic target, especially for guiding PARP inhibitor use beyond BRCA-mutated tumors.

Intriguingly, thedownregulation of SIX5 exhibited inhibitory effects on GBM cell growth in vitro, which were partially reversed by the overexpression of EXO1. In conclusion, the interplay between SIX5 and EXO1 emerges as a critical axis driving GBM development, shedding light on potential mechanisms for targeted interventions in combating this aggressive malignancy.

In summary, our results indicate a marked elevation in EXO1 expression levels within gliomas, which correlates strongly with clinical pathological characteristics and unfavorable prognosis. Moreover, EXO1 emerges as a promising candidate biomarker and potential therapeutic target for glioma, likely playing a critical role in mediating immune infiltration within this malignancy.

EXO1 exhibits multidimensional roles in female-related cancers as a prognostic biomarker and potentially influences tumor immune therapy responses and drug sensitivities. Further studies are needed to fully understand the complex mechanisms underlying these associations and to explore potential therapeutic strategies targeting EXO1.

These findings provide valuable insights into the potential of EXO1 as a biomarker and therapeutic target, as well as its role in determining treatment response in cancer management. This information is crucial for guiding personalized cancer therapy and precision medicine.

Notably, elevated expression of KIF11, CCNB1, and PLK1 is associated with poor prognosis in patients with TNBC. These findings contribute to an improved understanding of the epigenetic molecular mechanisms underlying TNBC progression and highlight novel biomarkers that may enhance the accuracy of TNBC diagnosis and provide potential targets for therapeutic intervention.

Importantly, immunogenomic analyses revealed EXO1's significant role in modulating the tumor microenvironment, as it is associated with immune cell infiltration and cytokine expression, suggesting its involvement in tumor immunology and immune response regulation. These results implied that EXO1 as a significant biomarker with prognostic and diagnostic potential across various malignancies, suggesting its potential as a therapeutic target and its involvement in immunomodulatory processes within the tumor microenvironment.

EXO1 expression was correlated with the infiltration of immune cells, and high expression of EXO1 was an adverse effect on LUAD patients receiving anti-PD-1/PD-L1 immunotherapy. Moreover, patients with EXO1 mutation had worse DSS, DFI and PFI.

This study identified ten hub genes associated with the initiation and progression of LUAD. Additionally, EXO1 may serve as a prognostic marker for LUAD patients, offering new perspectives for clinical treatments.

Analysis of 150 genes related to EXO1 demonstrate an enrichment in processes such as cell cycle regulation, DNA damage repair, and relevant signaling pathways, suggesting a possible mechanism through which EXO1 may facilitate tumor development. This study offers a deep insight into the role of EXO1 in different types of human cancers, indicating that EXO1 could act as an important prognostic biomarker and a therapeutic target for certain types of cancer.

This study unveils a novel regulatory pathway involving EXO1/Polη/Polι axis and miR-3163, providing insights into CSLCs regulation in NSCLC. EXO1/Polη/Polι axis targeted by miR-3163, resulting in the inhibition of cell growth and induction of apoptosis in NSCLC CSLCs.

These data provide a strong rationale for the therapy studies using PCNA-I1S or R9-AR-PIP in combination with X-ray radiation against CRPC tumors in preclinical models.